Objective To explore the inhibitory effect of 17-DMAG on the growth and angiogenesis of PD-1 humanized mouse liver cancer transplantation tumors. Methods 30 PD-1 humanized mice were selected, and a human HepG2 cell suspension was injected into the subcutaneous tissue of the right inguinal region to construct a human liver cancer transplant tumor model. Tumor-bearing humanized mice were randomly divided into three groups ( 10 mice per group): ① model group (injected with 10 mg / kg of physiological saline), ② 17-DMAG group (intraperitoneal injection of 17-DMAG at 25 mg / kg, 3 times/ week), and ③ cisplatin group ( intraperitoneal injection of 20 mg / kg, 2 times per week). The experiment lasted for 4 weeks. After injection, the length and shortest diameter of humanized mouse transplanted tumors were measured to calculate the volume, and tumor mass was measured to calculate the tumor inhibition rate. At the same time, immunohistochemical method were used to detect the expression of CD31 ( tumor microvessel density, MVD) and vascular endothelial growth factor (VEGF) in tumor tissue. Results The tumor volume and mass of the 17-DMAG group and cisplatin group were significantly reduced compared to those of the model group (P<0. 05), and the tumor inhibition rate of the 17-DMAG group was slightly higher than that of the cisplatin group. However, there were no significant differences in tumor mass, volume, and tumor inhibition rate between the 17-DMAG group and cisplatin group. The number of MVD-labeled microvessels and level of VEGF expression in the 17-DMAG group and cisplatin group were lower than those in the model group ( P<0. 05), and those of the 17-DMAG group were also lower than those in the cisplatin group (P<0. 05). Conclusions 17-DMAG can inhibit the growth of humanized mouse liver cancer xenografts by reducing the expression of VEGF in liver cancer xenograft tissue, thereby inhibiting the generation of tumor neovascularization.